Translational repression of Ccl5 and Cxcl10 by 4E-BP1 and 4E-BP2 restrains the ability of mouse macrophages to induce migration of activated T cells.
Identifieur interne : 000186 ( Main/Exploration ); précédent : 000185; suivant : 000187Translational repression of Ccl5 and Cxcl10 by 4E-BP1 and 4E-BP2 restrains the ability of mouse macrophages to induce migration of activated T cells.
Auteurs : Mirtha William [Canada] ; Louis-Philippe Leroux [Canada] ; Visnu Chaparro [Canada] ; Tyson E. Graber [Canada] ; Tommy Alain [Canada] ; Maritza Jaramillo [Canada]Source :
- European journal of immunology [ 1521-4141 ] ; 2019.
Descripteurs français
- KwdFr :
- Activation des lymphocytes (MeSH), Animaux (MeSH), Biosynthèse des protéines (MeSH), Cellules cultivées (MeSH), Chimiokine CCL5 (génétique), Chimiokine CXCL10 (génétique), Complexe-1 cible mécanistique de la rapamycine (métabolisme), Différenciation cellulaire (MeSH), Facteurs d'initiation eucaryotes (génétique), Facteurs d'initiation eucaryotes (métabolisme), Lymphocytes T (immunologie), Macrophages (immunologie), Maturation post-traductionnelle des protéines (MeSH), Mouvement cellulaire (MeSH), Protéines adaptatrices de la transduction du signal (génétique), Protéines adaptatrices de la transduction du signal (métabolisme), Protéines du cycle cellulaire (génétique), Protéines du cycle cellulaire (métabolisme), Répression épigénétique (MeSH), Souris (MeSH), Souris knockout (MeSH), Transduction du signal (MeSH).
- MESH :
- génétique : Chimiokine CCL5, Chimiokine CXCL10, Facteurs d'initiation eucaryotes, Protéines adaptatrices de la transduction du signal, Protéines du cycle cellulaire.
- immunologie : Lymphocytes T, Macrophages.
- métabolisme : Complexe-1 cible mécanistique de la rapamycine, Facteurs d'initiation eucaryotes, Protéines adaptatrices de la transduction du signal, Protéines du cycle cellulaire.
- Activation des lymphocytes, Animaux, Biosynthèse des protéines, Cellules cultivées, Différenciation cellulaire, Maturation post-traductionnelle des protéines, Mouvement cellulaire, Répression épigénétique, Souris, Souris knockout, Transduction du signal.
English descriptors
- KwdEn :
- Adaptor Proteins, Signal Transducing (genetics), Adaptor Proteins, Signal Transducing (metabolism), Animals (MeSH), Cell Cycle Proteins (genetics), Cell Cycle Proteins (metabolism), Cell Differentiation (MeSH), Cell Movement (MeSH), Cells, Cultured (MeSH), Chemokine CCL5 (genetics), Chemokine CXCL10 (genetics), Epigenetic Repression (MeSH), Eukaryotic Initiation Factors (genetics), Eukaryotic Initiation Factors (metabolism), Lymphocyte Activation (MeSH), Macrophages (immunology), Mechanistic Target of Rapamycin Complex 1 (metabolism), Mice (MeSH), Mice, Knockout (MeSH), Protein Biosynthesis (MeSH), Protein Processing, Post-Translational (MeSH), Signal Transduction (MeSH), T-Lymphocytes (immunology).
- MESH :
- chemical , genetics : Adaptor Proteins, Signal Transducing, Cell Cycle Proteins, Chemokine CCL5, Chemokine CXCL10, Eukaryotic Initiation Factors.
- chemical , metabolism : Adaptor Proteins, Signal Transducing, Cell Cycle Proteins, Eukaryotic Initiation Factors, Mechanistic Target of Rapamycin Complex 1.
- immunology : Macrophages, T-Lymphocytes.
- Animals, Cell Differentiation, Cell Movement, Cells, Cultured, Epigenetic Repression, Lymphocyte Activation, Mice, Mice, Knockout, Protein Biosynthesis, Protein Processing, Post-Translational, Signal Transduction.
Abstract
Signaling through the mechanistic target of rapamycin complex 1 (mTORC1) is a major regulatory node of pro-inflammatory mediator production by macrophages (MΦs). However, it is still unclear whether such regulation relies on selective translational control by two of the main mTORC1 effectors, the eIF4E-binding proteins 1 and 2 (4E-BP1/2). By comparing translational efficiencies of immune-related transcripts of MΦs from WT and 4E-BP1/2 double-KO (DKO) mice, we found that translation of mRNAs encoding the pro-inflammatory chemokines CCL5 and CXCL10 is controlled by 4E-BP1/2. Macrophages deficient in 4E-BP1/2 produced higher levels of CCL5 and CXCL10 upon LPS stimulation, which enhanced chemoattraction of activated T cells. Consistent with this, treatment of WT cells with mTORC1 inhibitors promoted the activation of 4E-BP1/2 and reduced CCL5 and CXCL10 secretion. In contrast, the phosphorylation status of eIF4E did not affect the synthesis of these chemokines since MΦs derived from mice harboring a non-phosphorylatable form of the protein produced similar levels of CCL5 and CXCL10 to WT counterparts. These data provide evidence that the mTORC1-4E-BP1/2 axis contributes to regulate the production of chemoattractants by MΦs by limiting translation efficiency of Ccl5 and Cxcl10 mRNAs, and suggest that 4E-BP1/2 act as immunological safeguards by fine-tuning inflammatory responses in MΦs.
DOI: 10.1002/eji.201847857
PubMed: 31032899
Affiliations:
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Graber</name><affiliation wicri:level="1"><nlm:affiliation>Children's Hospital of Eastern Ontario Research Institute, Ottawa, Ontario, Canada.</nlm:affiliation><country xml:lang="fr">Canada</country><wicri:regionArea>Children's Hospital of Eastern Ontario Research Institute, Ottawa, Ontario</wicri:regionArea><wicri:noRegion>Ontario</wicri:noRegion></affiliation></author><author><name sortKey="Alain, Tommy" sort="Alain, Tommy" uniqKey="Alain T" first="Tommy" last="Alain">Tommy Alain</name><affiliation wicri:level="1"><nlm:affiliation>Children's Hospital of Eastern Ontario Research Institute, Ottawa, Ontario, Canada.</nlm:affiliation><country xml:lang="fr">Canada</country><wicri:regionArea>Children's Hospital of Eastern Ontario Research Institute, Ottawa, Ontario</wicri:regionArea><wicri:noRegion>Ontario</wicri:noRegion></affiliation><affiliation wicri:level="1"><nlm:affiliation>Department of Biochemistry, Microbiology and Immunology, University of Ottawa, Ottawa, Ontario, Canada.</nlm:affiliation><country xml:lang="fr">Canada</country><wicri:regionArea>Department of Biochemistry, Microbiology and Immunology, University of Ottawa, Ottawa, Ontario</wicri:regionArea><wicri:noRegion>Ontario</wicri:noRegion></affiliation></author><author><name sortKey="Jaramillo, Maritza" sort="Jaramillo, Maritza" uniqKey="Jaramillo M" first="Maritza" last="Jaramillo">Maritza Jaramillo</name><affiliation wicri:level="1"><nlm:affiliation>INRS - Institut Armand-Frappier, Laval, Quebec, Canada.</nlm:affiliation><country xml:lang="fr">Canada</country><wicri:regionArea>INRS - Institut Armand-Frappier, Laval, Quebec</wicri:regionArea><wicri:noRegion>Quebec</wicri:noRegion></affiliation></author></analytic><series><title level="j">European journal of immunology</title><idno type="eISSN">1521-4141</idno><imprint><date when="2019" type="published">2019</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Adaptor Proteins, Signal Transducing (genetics)</term><term>Adaptor Proteins, Signal Transducing (metabolism)</term><term>Animals (MeSH)</term><term>Cell Cycle Proteins (genetics)</term><term>Cell Cycle Proteins (metabolism)</term><term>Cell Differentiation (MeSH)</term><term>Cell Movement (MeSH)</term><term>Cells, Cultured (MeSH)</term><term>Chemokine CCL5 (genetics)</term><term>Chemokine CXCL10 (genetics)</term><term>Epigenetic Repression (MeSH)</term><term>Eukaryotic Initiation Factors (genetics)</term><term>Eukaryotic Initiation Factors (metabolism)</term><term>Lymphocyte Activation (MeSH)</term><term>Macrophages (immunology)</term><term>Mechanistic Target of Rapamycin Complex 1 (metabolism)</term><term>Mice (MeSH)</term><term>Mice, Knockout (MeSH)</term><term>Protein Biosynthesis (MeSH)</term><term>Protein Processing, Post-Translational (MeSH)</term><term>Signal Transduction (MeSH)</term><term>T-Lymphocytes (immunology)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Activation des lymphocytes (MeSH)</term><term>Animaux (MeSH)</term><term>Biosynthèse des protéines (MeSH)</term><term>Cellules cultivées (MeSH)</term><term>Chimiokine CCL5 (génétique)</term><term>Chimiokine CXCL10 (génétique)</term><term>Complexe-1 cible mécanistique de la rapamycine (métabolisme)</term><term>Différenciation cellulaire (MeSH)</term><term>Facteurs d'initiation eucaryotes (génétique)</term><term>Facteurs d'initiation eucaryotes (métabolisme)</term><term>Lymphocytes T (immunologie)</term><term>Macrophages (immunologie)</term><term>Maturation post-traductionnelle des protéines (MeSH)</term><term>Mouvement cellulaire (MeSH)</term><term>Protéines adaptatrices de la transduction du signal (génétique)</term><term>Protéines adaptatrices de la transduction du signal (métabolisme)</term><term>Protéines du cycle cellulaire (génétique)</term><term>Protéines du cycle cellulaire (métabolisme)</term><term>Répression épigénétique (MeSH)</term><term>Souris (MeSH)</term><term>Souris knockout (MeSH)</term><term>Transduction du signal (MeSH)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Adaptor Proteins, Signal Transducing</term><term>Cell Cycle Proteins</term><term>Chemokine CCL5</term><term>Chemokine CXCL10</term><term>Eukaryotic Initiation Factors</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Adaptor Proteins, Signal Transducing</term><term>Cell Cycle Proteins</term><term>Eukaryotic Initiation Factors</term><term>Mechanistic Target of Rapamycin Complex 1</term></keywords><keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Chimiokine CCL5</term><term>Chimiokine CXCL10</term><term>Facteurs d'initiation eucaryotes</term><term>Protéines adaptatrices de la transduction du signal</term><term>Protéines du cycle cellulaire</term></keywords><keywords scheme="MESH" qualifier="immunologie" xml:lang="fr"><term>Lymphocytes T</term><term>Macrophages</term></keywords><keywords scheme="MESH" qualifier="immunology" xml:lang="en"><term>Macrophages</term><term>T-Lymphocytes</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Complexe-1 cible mécanistique de la rapamycine</term><term>Facteurs d'initiation eucaryotes</term><term>Protéines adaptatrices de la transduction du signal</term><term>Protéines du cycle cellulaire</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Cell Differentiation</term><term>Cell Movement</term><term>Cells, Cultured</term><term>Epigenetic Repression</term><term>Lymphocyte Activation</term><term>Mice</term><term>Mice, Knockout</term><term>Protein Biosynthesis</term><term>Protein Processing, Post-Translational</term><term>Signal Transduction</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Activation des lymphocytes</term><term>Animaux</term><term>Biosynthèse des protéines</term><term>Cellules cultivées</term><term>Différenciation cellulaire</term><term>Maturation post-traductionnelle des protéines</term><term>Mouvement cellulaire</term><term>Répression épigénétique</term><term>Souris</term><term>Souris knockout</term><term>Transduction du signal</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Signaling through the mechanistic target of rapamycin complex 1 (mTORC1) is a major regulatory node of pro-inflammatory mediator production by macrophages (MΦs). However, it is still unclear whether such regulation relies on selective translational control by two of the main mTORC1 effectors, the eIF4E-binding proteins 1 and 2 (4E-BP1/2). By comparing translational efficiencies of immune-related transcripts of MΦs from WT and 4E-BP1/2 double-KO (DKO) mice, we found that translation of mRNAs encoding the pro-inflammatory chemokines CCL5 and CXCL10 is controlled by 4E-BP1/2. Macrophages deficient in 4E-BP1/2 produced higher levels of CCL5 and CXCL10 upon LPS stimulation, which enhanced chemoattraction of activated T cells. Consistent with this, treatment of WT cells with mTORC1 inhibitors promoted the activation of 4E-BP1/2 and reduced CCL5 and CXCL10 secretion. In contrast, the phosphorylation status of eIF4E did not affect the synthesis of these chemokines since MΦs derived from mice harboring a non-phosphorylatable form of the protein produced similar levels of CCL5 and CXCL10 to WT counterparts. These data provide evidence that the mTORC1-4E-BP1/2 axis contributes to regulate the production of chemoattractants by MΦs by limiting translation efficiency of Ccl5 and Cxcl10 mRNAs, and suggest that 4E-BP1/2 act as immunological safeguards by fine-tuning inflammatory responses in MΦs.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">31032899</PMID><DateCompleted><Year>2020</Year><Month>05</Month><Day>27</Day></DateCompleted><DateRevised><Year>2020</Year><Month>05</Month><Day>27</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1521-4141</ISSN><JournalIssue CitedMedium="Internet"><Volume>49</Volume><Issue>8</Issue><PubDate><Year>2019</Year><Month>08</Month></PubDate></JournalIssue><Title>European journal of immunology</Title><ISOAbbreviation>Eur J Immunol</ISOAbbreviation></Journal><ArticleTitle>Translational repression of Ccl5 and Cxcl10 by 4E-BP1 and 4E-BP2 restrains the ability of mouse macrophages to induce migration of activated T cells.</ArticleTitle><Pagination><MedlinePgn>1200-1212</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1002/eji.201847857</ELocationID><Abstract><AbstractText>Signaling through the mechanistic target of rapamycin complex 1 (mTORC1) is a major regulatory node of pro-inflammatory mediator production by macrophages (MΦs). However, it is still unclear whether such regulation relies on selective translational control by two of the main mTORC1 effectors, the eIF4E-binding proteins 1 and 2 (4E-BP1/2). By comparing translational efficiencies of immune-related transcripts of MΦs from WT and 4E-BP1/2 double-KO (DKO) mice, we found that translation of mRNAs encoding the pro-inflammatory chemokines CCL5 and CXCL10 is controlled by 4E-BP1/2. Macrophages deficient in 4E-BP1/2 produced higher levels of CCL5 and CXCL10 upon LPS stimulation, which enhanced chemoattraction of activated T cells. Consistent with this, treatment of WT cells with mTORC1 inhibitors promoted the activation of 4E-BP1/2 and reduced CCL5 and CXCL10 secretion. In contrast, the phosphorylation status of eIF4E did not affect the synthesis of these chemokines since MΦs derived from mice harboring a non-phosphorylatable form of the protein produced similar levels of CCL5 and CXCL10 to WT counterparts. These data provide evidence that the mTORC1-4E-BP1/2 axis contributes to regulate the production of chemoattractants by MΦs by limiting translation efficiency of Ccl5 and Cxcl10 mRNAs, and suggest that 4E-BP1/2 act as immunological safeguards by fine-tuning inflammatory responses in MΦs.</AbstractText><CopyrightInformation>© 2019 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>William</LastName><ForeName>Mirtha</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>INRS - Institut Armand-Frappier, Laval, Quebec, Canada.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Leroux</LastName><ForeName>Louis-Philippe</ForeName><Initials>LP</Initials><Identifier Source="ORCID">0000-0002-9736-1827</Identifier><AffiliationInfo><Affiliation>INRS - Institut Armand-Frappier, Laval, Quebec, Canada.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Chaparro</LastName><ForeName>Visnu</ForeName><Initials>V</Initials><Identifier Source="ORCID">0000-0001-6880-9234</Identifier><AffiliationInfo><Affiliation>INRS - Institut Armand-Frappier, Laval, Quebec, Canada.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Graber</LastName><ForeName>Tyson E</ForeName><Initials>TE</Initials><AffiliationInfo><Affiliation>Children's Hospital of Eastern Ontario Research Institute, Ottawa, Ontario, Canada.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Alain</LastName><ForeName>Tommy</ForeName><Initials>T</Initials><AffiliationInfo><Affiliation>Children's Hospital of Eastern Ontario Research Institute, Ottawa, Ontario, Canada.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Biochemistry, Microbiology and Immunology, University of Ottawa, Ottawa, Ontario, Canada.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Jaramillo</LastName><ForeName>Maritza</ForeName><Initials>M</Initials><Identifier Source="ORCID">0000-0002-1910-5684</Identifier><AffiliationInfo><Affiliation>INRS - Institut Armand-Frappier, Laval, Quebec, Canada.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2019</Year><Month>05</Month><Day>06</Day></ArticleDate></Article><MedlineJournalInfo><Country>Germany</Country><MedlineTA>Eur J Immunol</MedlineTA><NlmUniqueID>1273201</NlmUniqueID><ISSNLinking>0014-2980</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D048868">Adaptor Proteins, Signal Transducing</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C503460">Ccl5 protein, mouse</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D018797">Cell Cycle Proteins</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D018946">Chemokine CCL5</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D054357">Chemokine CXCL10</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C485433">Cxcl10 protein, mouse</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C499527">Eif4ebp1 protein, mouse</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C491255">Eif4ebp2 protein, mouse</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D039642">Eukaryotic Initiation Factors</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 2.7.11.1</RegistryNumber><NameOfSubstance UI="D000076222">Mechanistic Target of Rapamycin Complex 1</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D048868" MajorTopicYN="N">Adaptor Proteins, Signal Transducing</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D018797" MajorTopicYN="N">Cell Cycle Proteins</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D002454" MajorTopicYN="N">Cell Differentiation</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D002465" MajorTopicYN="N">Cell Movement</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D002478" MajorTopicYN="N">Cells, Cultured</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D018946" MajorTopicYN="N">Chemokine CCL5</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D054357" MajorTopicYN="N">Chemokine CXCL10</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D063185" MajorTopicYN="N">Epigenetic Repression</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D039642" MajorTopicYN="N">Eukaryotic Initiation Factors</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008213" MajorTopicYN="N">Lymphocyte Activation</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008264" MajorTopicYN="N">Macrophages</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="Y">immunology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000076222" MajorTopicYN="N">Mechanistic Target of Rapamycin Complex 1</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D051379" MajorTopicYN="N">Mice</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D018345" MajorTopicYN="N">Mice, Knockout</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D014176" MajorTopicYN="N">Protein Biosynthesis</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D011499" MajorTopicYN="N">Protein Processing, Post-Translational</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D015398" MajorTopicYN="N">Signal Transduction</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D013601" MajorTopicYN="N">T-Lymphocytes</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="Y">immunology</QualifierName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="Y">4E-BP</Keyword><Keyword MajorTopicYN="Y">chemokines</Keyword><Keyword MajorTopicYN="Y">mRNA translation</Keyword><Keyword MajorTopicYN="Y">mTOR</Keyword><Keyword MajorTopicYN="Y">macrophages</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2018</Year><Month>08</Month><Day>09</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2019</Year><Month>04</Month><Day>09</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2019</Year><Month>04</Month><Day>23</Day></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2019</Year><Month>4</Month><Day>30</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2020</Year><Month>5</Month><Day>28</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2019</Year><Month>4</Month><Day>30</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">31032899</ArticleId><ArticleId IdType="doi">10.1002/eji.201847857</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list><country><li>Canada</li></country></list><tree><country name="Canada"><noRegion><name sortKey="William, Mirtha" sort="William, Mirtha" uniqKey="William M" first="Mirtha" last="William">Mirtha William</name></noRegion><name sortKey="Alain, Tommy" sort="Alain, Tommy" uniqKey="Alain T" first="Tommy" last="Alain">Tommy Alain</name><name sortKey="Alain, Tommy" sort="Alain, Tommy" uniqKey="Alain T" first="Tommy" last="Alain">Tommy Alain</name><name sortKey="Chaparro, Visnu" sort="Chaparro, Visnu" uniqKey="Chaparro V" first="Visnu" last="Chaparro">Visnu Chaparro</name><name sortKey="Graber, Tyson E" sort="Graber, Tyson E" uniqKey="Graber T" first="Tyson E" last="Graber">Tyson E. Graber</name><name sortKey="Jaramillo, Maritza" sort="Jaramillo, Maritza" uniqKey="Jaramillo M" first="Maritza" last="Jaramillo">Maritza Jaramillo</name><name sortKey="Leroux, Louis Philippe" sort="Leroux, Louis Philippe" uniqKey="Leroux L" first="Louis-Philippe" last="Leroux">Louis-Philippe Leroux</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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